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Biomedical subjects

H S Yu

Publications and source records attributed to H S Yu.

At least 163 records · Page 9Linked to original sources
PubMed1982

Regulation of melatonin in the retinae of guinea pigs: effect of environmental lighting.

We studied the effect of environmental lighting on the level of melatonin in the retinae of guinea pigs. Male pigmented guinea pigs were adapted to 12-hour light:12-hour dark (with lights on at 0600 hours) for 2 weeks. In experiment 1, two groups of animals were decapitated at 1600 and 0400 hours. Melatonin was extracted from retinae and quantified by radioimmunoassay. A diurnal rhythm of retinal melatonin level per pair of retinae was demonstrated. In experiment 2, one group was subjected to an extended dark period (lights remained off after 0600 hours) while the control group remained on the normal photoperiod on the day of sacrifice. Both groups were killed at 1200 hours. The retinal melatonin level in the group under extended dark period was significantly higher (P less than 0.05) than that of the control. In experiment 3, one group was exposed to an extended light period (lights remained on after 1800 hours) and the control group remained on the normal lighting schedule. Both groups were killed at 2400 hours. The retinal melatonin level in the group exposed to an extended light period was significantly lower (P less than 0.05) than that of the control. Thus, darkness induces an increase while light causes a decrease in retinal melatonin level.

Animals↗
PubMed1982

The level of N-acetylserotonin and melatonin in the brain of male rats: diurnal variations and effects of pinealectomy.

The levels of N-acetylserotonin and melatonin (n-acetyl-5-methoxytryptamine) in the rat brain were studied. Male rats were housed under a photoperiod of 12L:12D. After 2 weeks, the rats were sacrificed in light or in dark at 4-hour intervals round the clock. Brain melatonin and N-acetylserotonin were extracted by chloroform at greater than pH 10 and ethyl acetate at less than pH 3 respectively and quantified by radioimmunoassay. There was a circadian rhythm of brain melatonin (F less than 0.05) with a nadir at 1600 h and a zenith at 0400 h. Brain N-acetylserotonin, unlike brain melatonin, demonstrated no diurnal variation. Effects of pinealectomy on brain N-acetylserotonin and melatonin were also studied. Male rats were housed as noted. After 2 weeks, they were pinealectomized or shamoperated. The animals were killed in light or in dark 1 week after operation. The levels of brain melatonin at 2400 h and 0400 h were significantly lowered (P less than 0.05) following pineal removal. Pinealectomy, however, has no observable effect on the level of brain N-acetylserotonin. Our findings suggest that 1) there is a diurnal rhythm of brain melatonin, 2) the elevation of brain melatonin in the dark period is dependent on the pineal, 3) brain N-acetylserotonin has no diurnal variation, and 4) brain N-acetylserotonin is not affected by pinealectomy.

Animals↗
PubMed1982

Effect of light and darkness on the in vivo release of N-acetylserotonin and melatonin by the retina of guinea pigs.

The effect of light and darkness on the in vitro release of N-acetylserotonin and melatonin by the retina of male pigmented guinea pigs was studied. One group of the retina was incubated in light and the other group in dark for 12 h. Histological examination of the cultured retinal tissues indicated that the retinal cells appeared intact and healthy. N-acetylserotonin and melatonin released into the medium was extracted and then quantified by radioimmunoassay. The release of N-acetylserotonin and melatonin by retinas cultured in dark was significantly higher than those in light, indicating that the in vitro release of N-acetylserotonin and melatonin in increased by darkness or reduced by light. This supports the notion that the retina may be an important extrapineal source of melatonin in the circulation and may at least help to sustain diurnal rhythms of serum N-acetylserotonin and melatonin.

Animals↗
PubMed1981

A diurnal rhythm of N-acetylserotonin in the retina of rats.

Diurnal variation of N-acetylserotonin in the retina was studied in male rats housed under a photoperiod of 12 h light and 12 h darkness (lights on at 06.00 h) for two weeks. N-acetylserotonin was extracted from the retina by ethyl acetate at pH less than or equal to 3 and was determined by radioimmunoassay. There is a diurnal rhythm of N-acetylserotonin in the retina with high at night and low in the daytime. It is suggested that N-acetylserotonin in the retina may contribute partly to the levels of circulating N-acetylserotonin and may play a role in the regulation of photomechanical changes in the eye of rats.

Animals↗
PubMed1981

Persistence of circadian rhythms of melatonin and N-acetylserotonin in the serum of rats after pinealectomy.

To study the effect of pinealectomy (Px) on the rhythms of serum indoles, male rats were adapted to 12L:12D for 2 weeks after which half of them were Px. The animals were decapitated at 4-hour intervals 1 week after operation. Melatonin (Mel) and N-acetylserotonin (NAS) were extracted and quantified by RIA. The concentrations of serum Mel and NAS were significantly reduced after Px, suggesting that the pineal contributes a significant amount of these to the blood. However, circadian rhythms of them were not abolished by Px, indicating the existence of extrapineal sources at least one of which is capable of secreting Mel and NAS wih a diurnal rhythm. Retina is suspected to be an important source.

Animals↗
PubMed1981

Increase in the level of retinal melatonin and persistence of its diurnal rhythm in rats after pinealectomy.

To study the short- and long-term effects of pinealectomy on the level of retinal melatonin, male rats adapted to a photoperiod of 12 h light: 12 h darkness (with lights on at 06.00 h) were pinealectomy. In the short-term experiment, the rats were decapitated 1 week after pinealectomized. In the long-term experiment, 1 month was allowed for recovery. Melatonin was extracted from retinae and quantified by radioimmunoassay. A diurnal rhythm of retinal melatonin was found to persist after pinealectomy in both experiments. An increase in retinal melatonin was demonstrated 1 month after pinealectomy, indicating a compensatory effect on melatonin in the retinae of pinealectomized rats. Thus, biosynthesis of melatonin in the retina may be modulated through a negative feedback system.

Animals↗
PubMed1980

Melatonin in the retina of rats: a diurnal rhythm.

Melatonin was extracted by chloroform from the retina of the rat and measured by radioimmunoassay. In rats housed under a régime of 12 h light: 12 h darkness, melatonin content in the retina, like that in the pineal, serum and brain tissue, was high from midway through the dark to early in the period of light, and low from half-way through the light period to early in the period of darkness. A similar result was found in a second experiment. The existence of a diurnal rhythm of melatonin in the retina of rats as observed in this study is consistent with the suggestion that melatonin may regulate the diurnal rhythm of eye pigmentation in vertebrates.

Animals↗
PubMedDate not supplied

Interleukin 8 modulates interleukin-1 beta, interleukin-6 and tumor necrosis factor-alpha release from normal human mononuclear cells.

Recombinant human interleukin 8 (IL-8) enhanced the release of inflammatory cytokines including interleukin 1 beta (IL-1 beta), interleukin 6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) from normal human mononuclear cells in a dose-related manner (from 1 ng/ml to 10 ng/ml with a maximal effect at 5 ng/ml) when the cells incubated with IL-8 for 24 h. This cytokine-releasing activity of IL-8 is temperature-dependent and required protein synthesis since low temperature (4 degrees C) and cycloheximide (100 micrograms/ml) minimized the cytokine release from MNC. However, when IL-8 concentration was greater than 20 ng/ml, the cytokine release was suppressed. For further investigating the subcellular mechanism of the adverse effect of high dose IL-8 (20 ng/ml) in cytokine synthesis, human mononuclear cells (1 x 10(6)/ml) were stimulated with PHA (1 microgram/ml) in the presence of 20 ng/ml IL-8 for 3 days. We found not only [3H]thymidine incorporation of MNC was tremendously inhibited but DNA fragmentation appeared. Subsequently, the cell cycle of PHA-stimulated MNC retarded in the phase of G0/G1. These results suggest that in low concentration (5-10 ng/ml) IL-8 not only activated neutrophil phagocytosis but facilitated the release of inflammatory cytokines from mononuclear cells. Higher dose of IL-8 (more than 20 ng/ml) conversely suppressed these cytokine release from damaged cells by its cytotoxic effect. This newly found cytokine-releasing activity of IL-8 may play a role in the modulation of inflammation.

Cell Cycle↗
PubMedDate not supplied

Phase I clinical trial of curcumin, a chemopreventive agent, in patients with high-risk or pre-malignant lesions.

Curcumin (diferuloylmethane), a yellow substance from the root of the plant Curcuma longa Linn., has been demonstrated to inhibit carcinogenesis of murine skin, stomach, intestine and liver. However, the toxicology, pharmacokinetics and biologically effective dose of curcumin in humans have not been reported. This prospective phase-I study evaluated these issues of curcumin in patients with one of the following five high-risk conditions: 1) recently resected urinary bladder cancer; 2) arsenic Bowen's disease of the skin; 3) uterine cervical intraepithelial neoplasm (CIN); 4) oral leucoplakia; and 5) intestinal metaplasia of the stomach. Curcumin was taken orally for 3 months. Biopsy of the lesion sites was done immediately before and 3 months after starting curcumin treament. The starting dose was 500 mg/day. If no toxicity > or = grade II was noted in at least 3 successive patients, the dose was then escalated to another level in the order of 1,000, 2,000, 4,000, 8,000, and 12,000 mg/day. The concentration of curcumin in serum and urine was determined by high pressure liquid chromatography (HPLC). A total of 25 patients were enrolled in this study. There was no treatment-related toxicity up to 8,000 mg/day. Beyond 8,000 mg/day, the bulky volume of the drug was unacceptable to the patients. The serum concentration of curcumin usually peaked at 1 to 2 hours after oral intake of crucumin and gradually declined within 12 hours. The average peak serum concentrations after taking 4,000 mg, 6,000 mg and 8,000 mg of curcumin were 0.51 +/- 0.11 microM, 0.63 +/- 0.06 microM and 1.77 +/- 1.87 microM, respectively. Urinary excretion of curcumin was undetectable. One of 4 patients with CIN and 1 of 7 patients with oral leucoplakia proceeded to develop frank malignancies in spite of curcumin treatment. In contrast, histologic improvement of precancerous lesions was seen in 1 out of 2 patients with recently resected bladder cancer, 2 out of 7 patients of oral leucoplakia, 1 out of 6 patients of intestinal metaplasia of the stomach, I out of 4 patients with CIN and 2 out of 6 patients with Bowen's disease. In conclusion, this study demonstrated that curcumin is not toxic to humans up to 8,000 mg/day when taken by mouth for 3 months. Our results also suggest a biologic effect of curcumin in the chemoprevention of cancer.

Adult↗